This association between salt intake and Danshensu albuminuria was clear, even after adjusting for age and other factors. These findings suggest that salt intake is an important Clofentezine determinant of albuminuria in the adult Korean population. Several cross-sectional studies have shown an association between sodium intake and urinary albumin. The Framingham Offspring Study included 2,700 participants who underwent routine examinations between 1995 and 1998 and showed that the log urinary sodium index was associated positively with the log ACR and the urinary ACR in the fifth quintile of the urinary sodium index was twice as high as in the lowest quintile after adjusting for age, sex, diabetes, diuretic use, systolic and diastolic blood pressures, hypertension treatment, serum creatinine, and smoking. Vedovato et al. reported that switching from a low to a high sodium diet resulted in increases in blood pressure, body weight, and albuminuria in type 2 diabetics with microalbuminuria, but no changes occurred in type 2 diabetics without microalbuminuria. The finding of a significant association between sodium intake and albuminuria regardless of blood pressure in several studies suggested that the detrimental effect of sodium is not solely pressure-mediated. Some animal and human studies have shown that salt induced renal injury by increasing the systemic and intraglomerular blood pressures and by a pressure-independent mechanism. A high salt intake was linked to target organ injury, including left ventricular hypertrophy and renal fibrosis. Recently, inflammation has also been suggested to be related to salt intake and albuminuria. In primary hypertensive patients, the urinary sodium intake is correlated with both albuminuria and C-reactive protein, independent of any blood pressure effect. Conversely, a few studies found no association between sodium intake and albuminuria. In 2000, the Nurse’s Health Study reported that a high dietary intake of animal fat and red meat was associated with the presence of microalbuminuria, while the salt intake was not, although a higher salt intake was related to a decline in the eGFR. When interpreting this study, we should consider that the Nurse’s Health Study population was composed mostly of older Caucasian females with relatively high prevalences of hypertension and diabetes. The Coronary Artery Risk Development in Young Adults Study reported that during the 15-year follow-up, poor diet quality and obesity were associated with the development of microalbuminuria after multivariate adjustment, while smoking, low physical activity, fast food consumption, and sodium intake were not associated with the development of microalbuminuria. The reason for the discrepancy regarding the association of sodium intake with albuminuria is not clear. It might have been caused by the difference in population characteristics, including age, obesity, other cardiovascular risks, routine sodium intake in their community, and ethnicity. One of the main limitations of these two studies was the lack of urinary sodium measurements. A wellknown issue with dietary assessment instruments is the underreporting of nutrient intakes. In both studies, the sodium intake was measured using dietary recall. The recall method is less accurate than estimates based on urinary data. The equation that we used is recommended for estimating salt intake by the Japanese Society of Hypertension and has been validated in other studies.